Does the presence of hypoechoic lesions on transrectal ultrasound suggest a poor prognosis for patients with localized prostate cancer?

PURPOSE: The purpose of this study was to investigate the value of hypoechoic lesions on transrectal ultrasound (TRUS) as a prognostic factor for patients with localized prostate cancer. MATERIALS AND METHODS: The patients consisted of 71 patients with pT2N0M0 disease following radical prostatectomy between 2002 and 2008. The group with hypoechoic lesions was labeled group 1, whereas the group without hypoechoic lesions was labeled group 2. The presence of hypoechoic lesions on preoperative TRUS was analyzed as a prognostic factor along with several parameters, including preoperative factors and pathologic factors. The biochemical progression-free survival (BPFS) rate was compared between the two groups according to the presence of hypoechoic lesions on TRUS. RESULTS: A total of 35 patients had hypoechoic lesions on TRUS, whereas 36 had no hypoechoic lesions. Preoperative baseline characteristics were not significantly different between the two groups. In the univariate analysis, BPFS showed significant differences according to the presence of hypoechoic lesions on TRUS and the preoperative prostate-specific antigen level. The BPFS rates over the first 24 months were 97.0% in group 1 and 97.1% in group 2; however, the difference in the BPFS rate over 48 months significantly widened to 75.3% compared with 91.7%, respectively. Despite this finding, no significant independent prognostic factor for BPFS was found on multivariate analysis in this patient cohort. CONCLUSIONS: The presence of hypoechoic lesions on TRUS may suggest worse prognostic characteristics in pT2 prostate cancer. Further studies involving larger subject populations are needed to corroborate the significance of the presence of hypoechoic lesions as a prognostic factor.

Melatonin attenuates amyloid beta25-35-induced apoptosis in mouse microglial BV2 cells.

Melatonin has been reported to possess strong antioxidant actions, and is able to directly scavenge a variety of reactive oxygen species (ROS). The present study investigated whether melatonin possesses protective effects against Abeta-induced cytotoxicity in microglial cells. Cells treated with Abeta exhibited several characteristic features of apoptosis, while cells pre-treated with melatonin prior to exposure to Abeta showed a decrease in the occurrence of such apoptotic features. Several previous studies have demonstrated the involvement of ROS in Abeta-induced neurotoxicity, and ROS generated by Abeta have been reported to lead to the activation of nuclear factor-kappa B (NF-kappaB), a transcription factor; pre-treatment with melatonin in the present study reduced the level of Abeta-induced intracellular ROS generation, inhibited NF-kappaB activation, and suppressed the Abeta-induced increase in caspase-3 enzyme activity. In addition, it was found that pre-treatment with melatonin inhibits Abeta-induced increase in the levels of bax mRNA and that it enhances the level of bcl-2 expression. Based on these findings, the authors speculate that melatonin may provide an effective means of treatment for Alzheimer's disease through attenuation of Abeta-induced apoptosis.

Influence of maternal alcohol administration on c-Fos expression in the hippocampus of infant rats.

Maternal alcohol consumption during pregnancy is known to have a detrimental effect on the development of the fetus and its central nervous system (CNS) in particular. In the present study, the dose-dependence of the effect of maternal alcohol on hippocampal c-Fos expression, which is a marker of hippocampal neuronal activity and which is induced by a variety of stimuli, was examined in infant rats. In the present study, it was shown that expression of c-Fos in the hippocampus is decreased following treatment with alcohol in a dose-dependent fashion. Based on the results of the present study and the findings of other studies, it can be suggested that suppression of c-Fos expression in the hippocampus of infant rats with maternal alcohol administration mediates the associated developmental retardation and/or anomalies.

Administration of Folium mori extract decreases nitric oxide synthase expression in the hypothalamus of streptozotocin-induced diabetic rats.

Folium mori, the leaves of Morus alba L., has traditionally been used for the treatment of diabetic hyperglycemia. It has been shown to induce enhanced NOS expression in the hypothalamus of rats with streptozotocin (STZ)-induced diabetes. In the present study, the effect of Folium mori on the expression of nitric oxide synthase (NOS) in the hypothalamus of STZ-induced diabetic rats was investigated via nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry. Enhanced NAPDH-d expression was detected in the paraventricular nucleus, ventromedial hypothalamic nucleus, and lateral hypothalamic area of the hypothalamus in the STZ-induced diabetes group. Administration of the aqueous extract of Folium mori to rats with STZ-induced diabetes resulted in decreased NADPH-d positivity. These results suggest that Folium mori treatment is effective in curbing the desire for food under diabetic conditions via modulation of NO expression in the hypothalamus.

Alcohol and nicotine reduce cell proliferation and enhance apoptosis in dentate gyrus.

It is generally accepted that alcohol and nicotine affect learning ability and memory functions, especially in adolescents. In the present study, the effects of alcohol and nicotine on cell proliferation and apoptosis in the dentate gyrus of young rats were investigated. The results show that cell proliferation is suppressed by alcohol and nicotine. Furthermore, alcohol and nicotine increase the number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive cells. Based on the results presented in this study, it can be suggested that alcohol- and nicotine-related impairment in learning and memory functions may be due to alcohol- and nicotine-induced suppression of new cell formation and acceleration of apoptosis, especially during adolescence.

Alcohol and nicotine administration inhibits serotonin synthesis and tryptophan hydroxylase expression in dorsal and median raphe of young rats.

Serotonin (5-hydroxytryptamine, 5-HT) has been implicated in the pathophysiology of various neuropsychiatric disorders. In the present study, the effects of alcohol and nicotine on the synthesis of 5-HT and the expression of tryptophan hydroxylase (TPH), the rate-limiting enzyme of 5-HT synthesis, in the dorsal and median raphe of young rats were investigated via immunohistochemistry. The numbers of the 5-HT-positive and TPH-positive cells were reduced by alcohol and nicotine treatment in a dose-dependent manner. Based on the results, it can be suggested that the pathogenesis of alcohol- and nicotine-induced neuropsychological disorders involves alcohol- and nicotine-induced suppression of 5-HT synthesis and TPH expression in raphe, and that this may be of particular relevance in the consumption of alcohol and nicotine during adolescence.

Amiodarone induces apoptosis in L-132 human lung epithelial cell line.

To investigate whether amiodarone induces apoptosis in cells of the L-132 human lung epithelial cell line, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay, 4,6-diamidino-2-phenylindole staining, DNA fragmentation assay, reverse transcription-polymerase chain reaction, and casapse-3 enzyme assay were performed. Through morphological and biochemical analyses, it was demonstrated that L-132 cells treated with amiodarone exhibit several features of apoptosis. In addition, it was shown that amiodarone increases the mRNA levels of bax and caspase-3. Based on the results, amiodarone appears to activate specific intracellular death-related pathways, including possibly the bax-dependent caspase-3 activation pathway, and thus induce apoptosis in human lung epithelial cells.

l-myc Polymorphism in Gastric Cancer, Lung Cancer, and Hepatocellular Carcinoma.

PURPOSE: This study was performed to see if a particular polymorphism in the l-myc, a nuclear oncogene at the 1p32 locus, might be associated with greater risk of gastric cancer, lung cancer and hepatocellular carcinomas (HCC) in Korean patients. MATERIALS AND METHODS: Genomic DNA, derived from patients diagnosed with gastric cancer (n=57), lung cancer (n=39), HCC (n=35) and healthy individuals (n= 176), was examined. The l-myc polymorphism under study was visualized by PCR followed by EcoRI digestion. RESULTS: There was no significant difference in the distribution of the l-myc polymorphism genotypes and allele frequencies between the cancer patients and the controls. CONCLUSION: The l-myc polymorphism does not appear to be indicative of elevated risk of cancers of the stomach, lung and HCC.